• Search Research Projects
  • Search Researchers
  • How to Use
  1. Back to project page

2022 Fiscal Year Final Research Report

Analysis of transport mechanism of hemagglutinin of botulinum toxin complex to adherens junctions

Research Project

  • PDF
Project/Area Number 20K16240
Research Category

Grant-in-Aid for Early-Career Scientists

Allocation TypeMulti-year Fund
Review Section Basic Section 49050:Bacteriology-related
Research InstitutionKanazawa University

Principal Investigator

Amatsu Sho  金沢大学, 医学系, 助教 (90827346)

Project Period (FY) 2020-04-01 – 2023-03-31
Keywordsボツリヌス毒素 / ヘマグルチニン / 腸上皮細胞 / E-cadherin / カドヘリンフロー
Outline of Final Research Achievements

In this study, we have investigated that the extracellular trafficking pathway of hemagglutinin (HA) of botulinum toxin complex to reach adherens junctions (AJs). We demonstrated that HA binds to the basal cell surface and then moves to AJs where E-cadherin resides and forms cell-cell adhesion. In addition, we have revealed that RhoA inhibitor and myosin II inhibitor, which block actin-flow, inhibit the barrier disrupting activity of HA. These results suggest that HA is transported to AJs by actin-flow at the basal and lateral cell surfaces.

Free Research Field

細菌毒素

Academic Significance and Societal Importance of the Research Achievements

ボツリヌス毒素複合体のヘマグルチニン(HA)はE-cadherinに結合して腸管上皮細胞間バリアを破壊することで毒素の経口毒性を顕著に増大させる。本研究では、HAが腸管バリアを破壊するためにアドヘレンスジャンクションへ移動する細胞外輸送経路を解析した。その結果、in vitroにおいてアクチンフロー阻害剤はHAのバリア破壊活性を阻害することを明らかにした。今後、マウスを用いた試験により上記の阻害剤がボツリヌス毒素の経口毒性を低下させるのかを解析する予定である。

URL: 

Published: 2024-01-30  

Information User Guide FAQ News Terms of Use Attribution of KAKENHI

Powered by NII kakenhi